1. Field of the Invention
This invention relates to the field of neurosurgery, in particularly, a neurosurgical treatment for neurogenic disorders and, more specifically, to a neurosurgical method for the treatment of neurogenic conditions, including diabetes mellitus, by microvascular decompression of the medulla oblongata and viscera-related cranial nerves.
2. Background Art
Prior to the advance of microsurgical techniques, many intracranial procedures in the area of the brainstem were considered too risky and were not performed. With the introduction of the surgical microscope into neurosurgical practice, the intracranial vasculature and nearby neural structures could be visualized, thus facilitating the identification of subtle defects such as microvascular compression of the brainstem. Using microsurgical techniques, specific portions of the brain stem, cranial nerves, and minute blood vessels adjacent thereto can be manipulated to repair these defects.
One such microsurgical technique is microvascular decompression (MVD). In MVD, the surgeon typically identifies the locus of vascular compression, elevates the offending blood vessel or vessels from the surface of the affected neural tissue, and interposes a soft, biocompatible implant between the blood vessel and the neural tissue to maintain the decompression.
In general, as humans age, blood vessels tend to enlarge and may become ectatic, tortuous, and in many cases, sclerotic. To a large extent, the characteristics of a subject's vasculature are inherited and, therefore, heredity is considered to be a major factor in cerebrovascular pathophysiology. As certain subjects age, the intracranial blood vessels which surround the medulla oblongata such as the basilar and vertebral arteries, can press into the surface of the medulla. This compression can produce grooving of the medullary surface, which can alter the function of the anatomical entities innervated by the affected region of the medulla. Where arteries impinge upon the medulla and the cranial nerves, a pulsatile compression of those neural tissues is produced.
Vascular compression of certain cranial nerves has been found to create, or contribute to, numerous diseases or conditions, including for example, trigeminal neuralgia, audiovestibular dysfunction and hemifacial spasm, and glossopharyngeal neuralgia. For example, Jannetta discusses the etiologies, and treatments for, the aforementioned diseases in "Microsurgery of Cranial Nerve Cross-Compression," CLINICAL NEUROSURGERY, Chap. 26, pp. 607-15 (1979). Each disease can be considered a hyperactive dysfunction of the respective cranial nerves V, VII, VIII, IX, and X, most likely due to root entry zone abnormalities that are usually vascular in nature. There is evidence that brainstem compression, and vascular cross-compression at the root entry zone of cranial nerves, are related to a number of clinical syndromes. Microvascular decompression can be an extremely effective treatment for each of these diseases, with nerve function becoming greatly improved, if not fully normal, as a result.
Furthermore, pulsatile compression of the left lateral medulla oblongata by looping cerebral arteries at the base of the brain has been shown to cause neurogenic or "essential" hypertension. Jannetta, et al., describes the treatment of neurogenic hypertension using microvascular decompression of the left lateral medulla in "Essential Hypertension Caused by Arterial Compression of the Left Lateral Medulla: A Follow-Up," Perspec. Neurol. Surg., 3(1): 107-125 (1992).
It is believed that other diseases, including non-insulin-dependent diabetes mellitus (NIDDM), also may be caused or exacerbated by compressive cerebrovascular pathophysiology, particularly pulsatile vascular compression of the right lateral medulla. In general, diabetes mellitus is a syndrome resulting from a variable interaction of hereditary and environmental factors. It is characterized by abnormal insulin secretion, inappropriately elevated blood glucose levels, and a variety of end organ complications including nephropathy, retinopathy, neuropathy, and accelerated atherosclerosis. Patients with NIDDM may or may not use insulin for symptom control, but do not need it for survival. In NIDDM, tissue processes which control carbohydrate metabolism are believed to develop a decreased sensitivity to insulin over time. The progression of NIDDM is associated with increasing concentrations of blood glucose, and is coupled with a relative decrease in the rate of glucose-induced insulin secretion.
There is evidence that a relative excess of insulin, or hyperinsulinemia, may be associated with accelerated atherosclerosis, hypertension, hypertriglyceridemia, and reduced high-density lipoprotein cholesterol. Because insulin also is capable of causing insulin resistance, hyperglycemia can co-exist with hyperinsulinemia in patients with early NIDDM. Treatment of NIDDM typically includes weight control, regulation of diet, and the administration of either oral hypoglycemic agents or insulin. Such solutions are not entirely satisfactory because NIDDM patients acquire the sequelae typically associated with both hyperinsulinemia, e.g., accelerated atherosclerosis, hypertension, etc., and hyperglycemia, e.g., microvascular complications including nephropathy, retinopathy, neuropathy, etc. In general, it was thought although the progression of NIDDM could be slowed, but the ultimate effects of the disease were inexorable.
Although the cause of NIDDM is not fully understood, it is believed to be strongly influenced by hereditary factors due to its prevalence in particular families. Unlike insulin-dependent diabetes mellitus, which is thought to be caused by the autoimmune destruction of the insulin-producing cells of the pancreas, NIDDM is believed to be, at least at its inception, a decline and eventual failure of the neural and hormonal servomechanisms that promote euglycemia. Indeed, in early NIDDM, hyperglycemia and hypertension are epiphenomena.
Also, NIDDM is strongly associated with "apple" obesity, in which the subject develops a large abdomen with normal-sized limbs and lower torso. Heredity, too, plays a significant role in the incidence of "apple" obesity, in which the omentum enlarges, and which may be due to a breakdown in the fat storage servomechanism involving the abdominal adipose tissue and the omentum. Because insulin acts as a "fat-sparing" substance, the increased insulin levels of NIDDM also tend to promote obesity. A common link may exist between NIDDM and "apple" obesity because both appear to be products of a disruption of the internal milieu for glucose and fat servomechanisms and both the pancreas and omentum are innervated by fibers from cranial nerve X, the vagus nerve.
To the extent that the aforementioned servomechanisms promoting euglycemia can be restored prior to the exhaustion of the pancreas and the development of atherosclerosis and microvascular complications, NIDDM may be cured, or its effects be greatly ameliorated. At present, however, there is no commonly-accepted surgical procedure in use for the treatment of non-insulin-dependent diabetes mellitus.
What is needed then is a method and devices for treating a neuroendocrine disease, such as NIDDM, that is caused or exacerbated by microvascular compression of the brainstem tissue and associated cranial nerves.